Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cell‐state switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. Here, we show rapid induction of autophagy during temporary reprogramming in plants triggered by phytohormones, immune, and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely decay of previous cellular states and for tweaking the proteome to acclimate to the new conditions. Signatures of previous cellular programs thus persist in autophagy‐deficient cells, affecting cellular decision‐making. Concordantly, autophagy‐deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation during organogenesis. These observations indicate that autophagy mediates cell‐state switches that underlie somatic cell reprogramming in plants and possibly other organisms, and thereby promotes phenotypic plasticity.

SummaryIt is shown that AtCLCd negatively regulates Arabidopsis PTI, probably by interacting with the PRR signalling pathway. Its sequence indicates that AtCLCd encodes a chloride/proton exchanger.

Drought severely restricts plant production and global warming is further increasing drought stress for crops. Much information reveals the ability of individual microbes affecting plant stress tolerance. However, the effects of emergent bacterial community properties on plant drought tolerance remain largely unexplored. Here, we inoculated Arabidopsis plants in vivo with a four-species bacterial consortium (Stenotrophomonas rhizophila, Xanthomonas retroflexus, Microbacterium oxydans, and Paenibacillus amylolyticus, termed as SPMX), which is able to synergistically produce more biofilm biomass together than the sum of the four single-strain cultures, to investigate its effects on plant performance and rhizo-microbiota during drought. We found that SPMX remarkably improved Arabidopsis survival post 21-day drought whereas no drought-tolerant effect was observed when subjected to the individual strains, revealing emergent properties of the SPMX consortium as the underlying cause of the induced drought tolerance. The enhanced drought tolerance was associated with sustained chlorophyll content and endogenous abscisic acid (ABA) signaling. Furthermore, our data showed that the addition of SPMX helped to stabilize the diversity and structure of root-associated microbiomes, which potentially benefits plant health under drought. These SPMX-induced changes jointly confer an increased drought tolerance to plants. Our work may inform future efforts to engineer the emergent bacterial community properties to improve plant tolerance to drought.

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Turnip mosaic virus is a devastating potyvirus infecting many economically important brassica crops. In response to this, the plant host engages its RNA silencing machinery, involving AGO proteins, as a prominent strategy to restrain turnip mosaic virus (TuMV) infection. It has also been shown that the mRNA decay components DCP2 and VCS partake in viral infection suppression. Here, we report that the mRNA decapping components LSM1, PAT1, PATH1, and PATH2 are essential for TuMV infection. More specifically, lsm1a/lsm1b double mutants and pat1/path1/path2 triple mutants in summ2 background exhibit resistance to TuMV. Concurrently, we observed that TuMV interferes with the decapping function of LSM1 and PAT proteins as the mRNA-decay target genes UGT87A2 and ASL9 accumulate during TuMV infection. Moreover, as TuMV coat protein can be specifically found in complexes with PAT proteins but not LSM1, this suggests that TuMV “hijacks” decapping components via PAT proteins to support viral infection. [Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

11 Multicellular organisms perceive and transduce multiple cues to optimize developmental 12 reprogramming and cell state switching. Core transcription factors drive developmental changes, but 13 transitions also require the attenuation of previous states. Here, we demonstrate that the levels of 14 mRNAs of the LATERAL ORGAN BOUNDARIES DOMAIN (LBD)/ASYMMETRIC LEAVES9-LIKE 15 (ASL9) transcription factor are directly regulated by mRNA decapping. Capped ASL9 transcripts 16 accumulate in decapping deficient plants and ASL9 mRNAs are found together with decapping 17 components. Accumulation of ASL9 inhibits apical hook and lateral roots formation and interestingly, 18 exogenous auxin application restores apical and lateral roots in both ASL9 and mRNA decay deficient 19 mutants. Moreover, mutations in the cytokinin transcription factors type-B ARABIDOPSIS 20 RESPONSE REGULATORS (B-ARRs) ARR10 and ARR12 restore these developmental defects of 21 ASL9 overexpression. Thus, the mRNA decay machinery directly targets ASL9 transcripts for decay to 22 balance cytokinin/auxin responses during developmental reprogramming.23

Multicellular organisms perceive and transduce multiple cues to optimize development and cell state switching. Key transcription factors drive developmental changes, but transitions also require the attenuation of previous states and removal of negative regulators. Here, we report shared developmental defects in apical hook, primary and lateral root growth in multiple decapping deficient mutants. The mRNA levels of LATERAL ORGAN BOUNDARIES DOMAIN 3 (LBD3)/ASYMMETRIC LEAVES 2-LIKE 9 (ASL9) transcription factor are directly regulated by mRNA decapping machinery. More specifically, ASL9 transcripts accumulate in decapping deficient plants and can be found in complexes with decapping components. Accumulation of ASL9 inhibits apical hook, primary root growth and lateral root formation. Interestingly, exogenous auxin application restores lateral roots formation in both ASL9 over-expressors and mRNA decay-deficient mutants. Moreover, mutations in the cytokinin transcription factors type-B ARABIDOPSIS RESPONSE REGULATORS (B-ARRs) ARR10 and ARR12 restore the developmental defects caused by over-accumulation of capped ASL9 transcript upon ASL9 overexpression. Most importantly, loss-of-function of asl9 partially restores apical hook, primary root growth and lateral root formation in decapping deficient mutants. Thus, the mRNA decay machinery directly targets ASL9 transcripts for decay to balance cytokinin/auxin responses during development.

No abstract